Monday, 23 January 2017

Annexin V FITC.

An article published this year
in “CHEMISTRY AND PHYSICS OF LIPIDS” using ourAnnexin V FITC, by our
customers from Unidad de Biofísica (CSIC, UPV/EHU), and Departamento de
Bioquímica, Universidad del País Vasco, Bilbao, Spain, in the analysis of
Lipidomic profile of GM95 cell death induced by Clostridium perfringens
alpha-toxin. Congrats and Thanks.

Summary:

Clostridium perfringens alpha-toxin
(ATX) is considered as a prototype of cytotoxic bacterial phospholipases C, and
is the major virulence factor in C. perfringens-induced gas gangrene. It is known that, depending on the dose, ATX causes
membrane disruption and cytolysis or only limited hydrolysis of its substrates.
In the latter case, toxin activity leads to the unregulated generation of
bioactive lipids that can ultimately induce cell death. We have characterized
apoptosis and necrosis in highly ATX-sensitive, ganglioside-deficient cells
exposed to different concentrations of ATX and we have studied the lipidomic
profile of cells treated with ATX as compared to native cells to detect the
main changes in the lipidomic profile and the possible involvement of lipid
signals in cell death. ATX causes both apoptosis and necrosis, depending on
dose and time. ATX activates cell death, stimulating the release of cytochrome
C from mitochondria and the consequent activation of caspases-3. Moreover GM95
cells treated with ATX showed important lipidomic alterations, among them we
detected a general decrease in several phospholipid species and important
changes in lipids involved in programmed cell death e.g. ceramide. The data
suggest two different mechanisms of cell death caused by ATX, one leading to
(mainly saturated) glycerophospholipid hydrolysis related to an increase in
diacylglycerols and associated to membrane damage and necrosis, and a second
mechanism involving chiefly sphingomyelin hydrolysis and generation of
proapoptotic lipidic mediators such as ceramide, N-acylethanolamine and
saturated non-esterified fatty acids.